Continuing detailed qualitative and quantitative comparison of potassium-excess and sodium-lack contractures, in order to test more critically two working hypothesis: that the KCl contracture is mediated by an increased calcium influx into these fibers and the low sodium one by a decrease in calcium extrusion; that decreasing extracellular sodium concentration has dual effects (on depolarization-induced calcium influx and on calcium extrusion) the lower range of sodium concentrations (0-30mM) affecting primarily the latter process. Continuing a study of staircase in frog atrial muscle, to test, in particular, possible correlations between the slow inward current and beat-to-beat augmentation of contraction. Also to see if a stronger case for intracellular sodium accumulation, as the inotropic mediating event, can be made than in frog ventricle. Starting a systematic study of the inotropic effect of changes in extracellular potassium concentration, including: clear demonstration of voltage-independence of these inotropic effects over as large a range of potassium concentrations (above & below "normal" values) as will allow adequate voltage control during voltage clamp; quantitative analysis of the effect of increased and decreased extracellular potassium on the voltage-tension relationship: examination of potassium's inotropic effects under experimental conditions, including potassium-excess and sodium-lack contractures, as well as activation induced by voltage clamp depolarizations.